Dermoscopic Perspective of Pityriasis Versicolor in a Cross-Sectional Study

Abstract

Background:

Pityriasis versicolor is a common superficial fungal infection which is usually easily diagnosed with Wood’s lamp examination and 10% potassium hydroxide mount. However, these modalities have varying sensitivity and specificity.

Aims and Objectives:

This study aimed to ascertain the dermoscopic features of pityriasis versicolor lesionally as well as perilesionally using dermoscopy, a non-invasive diagnostic tool.

Materials and Methods:

In this cross-sectional study, consecutive patients with pityriasis versicolor underwent dermoscopic examination of lesions and 2 cm around lesions, noting lesional and perilesional features. Semi-objective grading of pigmentation, scaling, and vascularity was done. The association between parameters was determined using heat maps and violin plots with Kolmogorov–Smirnov test. Lesional analysis was performed since lesions at different sides showed disparate features.

Results:

A total of 353 lesions from 233 patients (males = 150/233; 64.38% and females = 84/234; 36.05%) were studied. On lesional dermoscopy, pigmentary and scaling abnormalities were universal. 258/353 (73.1%) of lesions showed vascular abnormalities. Perilesionally, scaling (223/353; 63.17%) followed by pigmentation (205/353; 58.07%) and vascular changes (111/353; 31.44%) constituted the most common dermoscopic abnormalities and were noted in 294/353 (83.29%) of lesions overall. Increased disease duration corresponded with increased intensity of perilesional pigmentation alterations, perifollicular (P = 0.04), and follicular scales (P = 0.02).

Conclusion:

Awareness of dermoscopic features could improve the diagnostic accuracy in doubtful cases of pityriasis versicolor. Vascular findings are common and may point to an underlying inflammatory pathogenesis. Perilesional findings constitute early dermoscopic features of pityriasis versicolor and hint at the need for treatment beyond the confines of lesions. Larger follow-up studies and research into immunopathogenesis may be of further benefit.

Introduction

Pityriasis versicolor (PV), a common superficial mycosis caused by Malassezia genus, presents with macules or patches of varied color, with characteristic fine, furfuraceous scaling which may be inconspicuous clinically.[1,2,3] Clinical diagnosis is by yellow fluorescence on Wood’s lamp. Confirmation is by 10% potassium hydroxide (KOH) mount. Dermoscopy is a useful, easy-to-use diagnostic tool in multiple dermatoses. However, dermoscopic studies in PV are relatively few. This study aimed to ascertain the dermoscopic patterns in PV.

Materials and Methods

Consecutive patients with PV (confirmed by 10% KOH mount) were recruited after written informed consent and ethics committee approval. Patients who had taken anti-fungal treatment or topical steroids in the last three months or had extensive scaly or pigmentary conditions were excluded. Demographic and clinical data were recorded. Lesional borders were demarcated by clinical examination and Wood’s lamp fluorescence (whichever was wider). Videodermoscopy was performed using a Dinolite videodermoscope (50x, 200x) of regional normal skin (negative control), a lesion, and 2 cm perilesionally (around the demarcated edge of lesions) at each site. Lesional and perilesional findings were classified into pigmentary, scaling, and vascular findings, and semi-objectively graded by three independent observers. Grade 0 implies no abnormality, grade 1 implies a just perceptible feature (or, in pigmentary disturbance, noticeable preservation of a normal pigment network) or occupying less than 25% of the dermoscopic field, and grade 2 implies prominent features (or, in pigmentary disturbance, severe accentuation/attenuation/absence of normal pigment network) and covering >25% of the dermoscopic field. Only if hyperpigmentation persisted after spirit swabbing, it was considered true hyperpigmentation. Skin markings and acrosyringeal orifices were also noted. Pigmentary contrast halo (CH) was defined as a clearly defined color opposite to the major lesional dermoscopic hue (e.g., hyperpigmentation around a dermoscopically hypopigmented lesion) which surrounded ≥50% of the lesion. The mere coexistence of hyperpigmentation and hypopigmentation on dermoscopy was not considered CH. The location of the features vis-à-vis hair follicles was recorded.

Statistical analysis

Means and percentages were calculated. Relationships between categorical variables were expressed in the form of heat maps. Violin plots were used to visualize distributions of continuous variables, and Kolmogorov–Smirnov (KS) test was used to ascertain significance levels. Differences between means were compared using an unpaired t test. Proportions were compared using Chi-square test. A significance threshold of P < 0.05 was used for all tests.

Results

A total of 353 lesions from 233 patients in Fitzpatrick skin types 4 (220/233; 94.42%) and 5 (13/233; 5.58%) were studied over one year. Males (150/233; 64.38%) outnumbered females (84/234; 36.05%). The mean age was 27.9 years (standard deviation: 13.06 years; range: 4 to 60 years). Disease duration averaged five months (range: 1 week to 5 years). Among patients, 5/233 (2.15%) were on immunosuppressive medications. Most patients (167/233; 71.67%) were asymptomatic. The remaining had mild pruritus. A single site was involved in 136/233 (58.3%) of patients. Truncal lesions were the most common (156/353; (44.1%)) followed by the upper limb (95/353; 26.91%). The upper back was most frequently involved (107/353; 21.25%). In children (58/233; 24.89% patients; 94/353; 26.63% lesions), facial lesions predominated (36/94; 38%) followed by truncal lesions (27/94; 29%). Patients presenting with hypopigmented PV were common (163/233; 69.96%) followed by hyperpigmented (67/233; 28.76%), mixed hypopigmented, and hyperpigmented (2/233; 0.86%) and erythematous variants (1/233; 0.43%). Out of lesions assessed, the trend was similar with preponderant hypopigmented lesions [Table 1]. There were no statistically significant differences in mean disease duration, number of sites affected or symptoms between patients with hypopigmented and hyperpigmented PV.

Table 1.

Lesional dermoscopic abnormalities (total=353)^a

Dermoscopic changes	Clinically hypopigmented lesions (67.99%; n=240)	Clinically hyperpigmented lesions (30.03%; n=106)	Clinically mixed lesions (0.85%; n=3)	Clinically erythematous lesions (1.13%; n=4)
PIGMENTARY CHANGES
Hypopigmentation	133 (55.42)	0	0	0
Hyperpigmentation	0	61 (57.55)	0	4 (100)
Mixed	107 (44.58)	45 (42.45)	3 (100)	0
Grade 1	110 (45.83)	33 (31.13)	1 (33.33)	3 (75)
Grade 2	130 (54.17)	73 (68.87)	2 (67.67)	1 (25)
HYPERPIGMENTARY CHANGESb,c
Regular network accentuation	21 (8.75)	12 (11.32)	3 (100)	0
Irregular network accentuation	77 (32.08)	63 (59.43)	0	1 (25)
Diffuse pigmentation	39 (16.25)	56 (52.83)	3 (100)	2 (50)
Small pigmentary dots	27 (11.25)	16 (15.09)	0	1 (25)
Large pigmentary dots (clods and blotches)	23 (9.58)	27 (25.47)	0	1 (25)
Interfollicular pigment abnormality	14 (5.83)	5 (4.72)	0	0
Perifollicular pigment abnormality	19 (7.92)	1 (0.94)	3 (100)	0
Combined interfollicular and perifollicular pigment abnormality	207 (86.25)	100 (94.34)	0	4 (100)
SCALING
Grade 1	152 (74.51%)	45 (42.45)	3 (100)	4 (100)
Grade 2	88 (36.67)	61 (57.55)	0	0
Crease	128 (53.33)	82 (77.36)	1	1 (25)
Interfollicular	177 (73.75)	78 (73.58)	0	4 (100)
Perifollicular	204 (85)	100 (94.34)	3	4 (100)
Follicular	195 (81.25)	78 (73.58)	3	3 (75)
VASCULAR FINDINGS
Grade 1	108 (45)	59	3 (100)	2 (50)
Grade 2	61 (25.42)	23	0	2 (50)
Blush	153 (63.75)	79 (74.53)	2 (67.67)	4 (100)
Liner vessels	69 (28.75)	25 (23.58)	1 (33.33)	4 (100)
Small dots	36 (15)	20 (18.87)	0	3 (75)
Large dots	19 (7.92)	14 (13.21)	0	1 (25)
Normal (grade 0)	71 (29.58)	24 (22.64)	0	0
FURROWS
Reduced	48 (20)	5 (4.72)	0	2 (50)
Accentuated	101 (42.08)	84 (79.25)	0	2 (50)
Normal	91 (37.92)	17 (16.04)	3 (100)	0
ACROSYRINGEUM
Less visualized	134 (55.83)	61 (57.55)	0	1 (25)
Accentuated	2 (0.83)	1 (0.94)	0	0
Normal	104 (43.33)	44 (41.51)	3 (100)	3 (75)

^aFigures in brackets indicate the percentage. ^bAll hypopigmented lesions with these features had coexistent hyperpigmentary features on dermoscopy. ^cHyperpigmented features on dermoscopy were not mutually exclusive

On lesional dermoscopy, 52/97 (53.6%) of patients with lesions on multiple sites had different findings at various sites. Therefore, lesional analysis (and not patient analysis) was performed. Pigmentary and scaling patterns were noted in all lesions [Table 1 and Figures 1 and 2]. While in most lesions, dermoscopic color alteration (hypo- or hyperpigmentation) corresponded to the clinical color, considerable proportions of patients in both groups had both pigmentary patterns. Irregular pigment network accentuation was the most common hyperpigmentary feature in clinically hypopigmented and hyperpigmented lesions, followed by diffuse pigmentation. Hyperpigmentary features were seen in 107/240 (44.6%) of clinically hypopigmented lesions. Multiple hyperpigmentary patterns were seen in 124/220 (56.4%) of lesions with a dermoscopic hyperpigmentary component comprising combinations of smaller and larger dots and pigment network accentuation. Combined perifollicular and interfollicular pigment network perturbance predominated. Dermoscopic scaling patterns comprised crease (double-edged), interfollicular non-crease, perifollicular (surrounding the hair follicle but not extending along it), and follicular (encasing the follicle for varying lengths) patterns. In both clinical types, perifollicular scaling was preponderant [Table 1]. In clinically hypopigmented lesions, follicular scaling was the next most frequent, whereas in clinically hyperpigmented lesions, crease scales were the next most common.

Figure 1.

Pigmentary changes on videodermoscopy (50x). Clinical images and dermoscopic images of regional uninvolved skin are on the left and right inset, respectively (a) Significantly effaced pigment network (gr 2 hypopigmentation) of a facial lesion of PV. Also note the subtle follicular, interfollicular scales, and blush (both grade 1) with attenuated acrosyringeal orifices (b) Subtle accentuation and thickening of regular pigment network in a clinically hyperpigmented lesion of PV. Note the sparing of furrows which appear relatively hypopigmented, and therefore, prominent. Mild (grade 1) scaling is noted along the furrows (circle), interfollicularly (arrow), around (square), and along hair follicles (triangle) (c) Combined prominent hypopigmentation with marked effacement of pigment network with irregular accentuation (grade 2 pigment alteration) in a clinically hypopigmented lesion. Also, note focal scales in the creases, interfollicularly and perifollicularly with subtle erythema (both grade 1) (d) Diffuse hyperpigmentation completely effacing the normal pigmentary network along with larger pigmentary dots (grade 2), prominent blush (grade 2), and fine branny scales along the creases, around and along the hair follicles (circle) (grade 1) in a clinically hyperpigmented lesion of PV on the neck (inset)

Figure 2.

Scaly (2a and b) and vascular (2c and d) changes on dermoscopy (50x). Clinical images and dermoscopic images of regional uninvolved skin are on the left and right inset, respectively (a) Subtle scales (grade 1) in interfollicular (boxes) and perifollicular (oval) locations (b) Predominant crease (double-edged) and interfollicular scaling (grade 2) and blush (c) Subtle blush (grade 1) with perifollicular and interfollicular grade 1 scales (d) Grade 2 blush, short linear vessels, and dots (top right inset; 200x magnification) of varying sizes with grade 1 perifollicular, interfollicular, and follicular scales

Dermoscopic vascular findings were noted in 258/353 (73.1%) of patients [Figures 2c and d]. The most common pattern was pink-red background (blush). Although commoner in hyperpigmented lesions, no statistical significance was noted in the proportion of clinically hypopigmented and hyperpigmented lesions with dermoscopic vascular features (P = 0.1).

Compared to normal regional skin, prominent furrows due to pigmentary changes/scales were noted in 187/353 (52.97%) [Figure 1b], attenuated in 55/353 (15.58%), and normal in 111/353 (31.44%) lesions. Acrosyringeal openings were attenuated in 196/353 (55.52%) [Figure 1a], prominent owing to surrounding hyperpigmentation in 3/353 (0.85%), and visualized normally in 154/353 (43.63%).

Perilesional dermoscopic features were noted in 294/353 (83.29%) lesions [Table 2 and Figure 3]. The most common was scaling (223/353; 63.17%) followed by pigmentary (205/353; 58.07%) and vascular (111/353; 31.44%) changes. These were more common around hypopigmented than hyperpigmented lesions (204/240; 85% versus 86/106; 81.1%, respectively). The face (14/48; 29.17%) followed by the neck (12/46; 26.09%) had a maximum proportion of perilesional abnormalities.

Table 2.

Perilesional dermoscopic features^a,b

Dermoscopic changes	Clinically hypopigmented lesions (67.99%; n=240)	Clinically hyperpigmented lesions (30.03%; n=106)	Clinically mixed lesions (0.85%; n=3)	Clinically erythematous lesions (1.13%; n=4)
PIGMENTARY CHANGES
Hypopigmentation	79 (32.92)	12 (11.32)	1 (33.33)	0
Hyperpigmentation	44 (18.33)	33 (31.13)	0	1 (25)
Mixed	26 (10.83)	7 (6.6)	2 (66.67)	0
Grade 1	124 (51.67)	46 (43.4)	1 (33.33)	0
Grade 2	25 (10.42)	6 (5.66)	2 (66.67)	1 (25)
Normal (grade 0)	91 (37.92)	54 (50.94)	0	3 (75)
HYPERPIGMENTARY CHANGESc
Regular network accentuation	27 (11.25)	7 (6.6)	0	0
Irregular network accentuation	31 (12.92)	25 (23.58)	2 (66.67)	0
Small pigmentary dots	4 (1.67)	0	0	0
Large pigmentary dots	9 (3.75)	4 (3.77)	0	0
Diffuse pigmentation	19 (7.92)	13 (12.26)	2 (66.67)	1 (25)
Interfollicular pigment abnormality	117 (48.75)	9 (8.49)	0	0
Perifollicular pigment abnormality	32 (13.33)	5 (4.72)	1 (33.33)	1 (25)
Combined interfollicular and perifollicular pigment abnormality	105 (43.75)	38 (35.85)	2 (66.67)	0
VASCULAR FINDINGS
Grade 1	66 (27.5)	29 (27.36)	3 (100)	1 (25)
Grade 2	7 (2.92)	5 (4.71)	0	0
Blush	60 (25)	30 (28.3)	0	1 (25)
Liner vessels	30 (12.5)	9 (8.49)	3 (100)	0
Smaller dots	4 (1.67)	0	0	0
Larger dots	4 (1.67)	3 (2.83)	2 (66.67)	0
Normal (grade 0)	167 (69.58)	72 (67.9)	0	3 (75)
SCALING
Grade 1	156 (65)	61 (57.55)	3 (100)	1 (25)
Grade 2	1 (0.42)	1 (0.94)	0	0
Crease	35 (14.58)	22 (20.75)	0	0
Interfollicular	92 (38.33)	33 (31.13)	2 (66.67)	1 (25)
Perifollicular	89 (37.08)	38 (35.85)	1 (33.33)	0
Follicular	106 (44.17)	30 (28.3)	2 (66.67)	0
Absent (grade 0)	83 (34.58)	44 (41.51)	0	3 (75)
FURROWS
Reduced	92 (38.33)	40 (37.74)	0	0
Accentuated	38 (15.83)	21 (19.81)	2 (66.67)	0
Normal	110 (45.83)	45 (42.45)	1 (33.33)	4 (100)
ACROSYRINGEUM
Less visualized	4 (1.67)	2 (0.97)	0	0
Accentuated	0	1 (0.94)	0	0
Normal	236 (98.33)	103 (97.17)	3 (100)	4 (100)

^aFigures in brackets indicate the percentage. ^bNo dermoscopic abnormalities 16.43% (58/353) lesions. ^cHyperpigmented features on dermoscopy were not mutually exclusive

Figure 3.

Perilesional changes on dermoscopy (50x). Clinical images of lesions are in the left inset and dermoscopic images of regional uninvolved skin are on the right inset (a) Prominent (grade 2) hypopigmentation around hypopigmented lesions on the face along with grade 1 blush (b) Accentuated irregular pigment network and blotchy pigmentation with hypopigmentation (grade 2) with perifollicular scales (circle) and interfollicular scales (rectangle) (grade 1) (c) Prominent grade 2 blush with subtle grade 1 interfollicular scales (d) A contrast halo of hyperpigmented network accentuation is noted around a folliculocentric hypopigmented scaly patch of pityriasis versicolor with follicular scale

Perilesionally, irregular pigmentary network accentuation constituted the most common pigmentary feature. Surrounding hypopigmented lesions, interfollicular pigmentary alteration was preponderant unlike hyperpigmented lesions around which combined perifollicular and interfollicular pigment alteration was common. Hyperpigmented CHs around dermoscopically hypopigmented lesions were found in 97/353 (27.48%) of lesions and vice versa in 1/353 (0.28%) of lesions.

Among scaling patterns, follicular scaling was common surrounding hypopigmented lesions. Perifollicular scaling was slightly common around clinically hyperpigmented lesions.

Perilesional vascular changes commonly comprised blush followed by linear vessels. No correlation between clinical symptoms and lesional/perilesional vascular findings were noted (P = 0.2 and 0.3, respectively). Comparison of the proportion of hypopigmented versus hyperpigmented lesions with perilesional pigmentation showed statistical significance (P = 0.02) with more changes around hypopigmented lesions. In scaling and vascular findings, no statistical significance (P = 0.7 and 0.8, respectively) was noted.

Perilesional acrosyringeal orifices were normal in 346/353 (98.02%), attenuated in 6/353 (1.7%), and prominent due to surrounding hyperpigmentation in 1/353 (0.28%) lesions. Furrows were normal in 334/353 (94.62%), widened in 10/353 (2.83%), and reduced/absent in 9/353 (2.55%) lesions.

Comparing proportions of lesions with perilesional grade 1 vascularity, a statistically significant increase was noted as the grade of perilesional scaling increased from 0 to 1. A significant increase in lesions with vascularity was noted as the lesional grade of scales increased from 1 to 2.

Apart from a slight predilection of follicular scale and grade 2 pigmentary alteration for the face, no site-specific differences in scaling were noted. The distribution of disease duration is significantly different when comparing populations with grade 1 versus grade 2 intensity of pigmentary disturbance perilesionally (P = 0.04) suggesting that grade 2 perilesional pigmentary disturbance is associated with a longer disease duration. Also, longer disease duration corresponded with the presence of grade 2 perilesional follicular and perifollicular scales (P = 0.02 and 0.04, respectively) [Figures 4 and 5].

Figure 4.

Distributions of disease duration are significant on the KS test (P = 0.02) when comparing the presence versus absence of perilesional follicular scales suggesting that longer disease duration is associated with this perilesional abnormality

Figure 5.

Distributions of disease duration are significant on the KS test (P = 0.04) when comparing the presence versus absence of perilesional perifollicular scales suggesting that longer disease duration is associated with this perilesional abnormality

Discussion

Pityriasis versicolor predominates in warm, humid climates. Although usually easy to diagnose and manage, owing to its varied manifestations, it may occasionally be confused with diverse skin diseases, especially in low prevalence settings or by the inexperienced clinician.[4,5,6,7] Accurate diagnosis is essential for appropriate therapy. Fluorescence on Wood’s lamp examination is often subjective and may be absent after sweating or bathing. Although specific, the KOH mount is not highly sensitive and is subject to variable interpretation.[3,8] Malassezia is lipophilic; therefore, culture requires oil-enriched media, which is time-consuming and not easily available.[3] Dermoscopy is an emerging diagnostic tool in PV. However, large-scale analyses of dermosocopic features including perilesional features, and descriptions of relationships between various observations are lacking. This study aimed to address these aspects.

The patients’ mean age and male preponderance were similar to previous Indian studies.[3,4,9,10,11] The most common site of involvement was the trunk, while in children, it was the face as described by Kaur.[3] Hypopigmented lesions were commoner, like previous studies in part owing to the contrast with background darker skin contributing to patient awareness.[3,4,9] Another factor was diseases such as vitiligo and leprosy, which resemble hypopigmented PV clinically, are prevalent in India, and are associated with patient anxiety. Hyperpigmented lesions are often noticed later by patients due to their higher Fitzpatrick skin type and are associated with a higher fungal load.[4]

Dermoscopically, pigmentary abnormalities were universal. The mixed interfollicular and perifollicular pigmentary disturbance was common, unlike Kaur who found more frequent perifollicular pigment alteration.[3] The roughly equal proportions (approaching 45%) of contrasting dermoscopic colors in clinically monochromatic lesions are probably owing to compensatory hypermelanosis or melanocyte consumption.[3,4] Hypopigmentary patterns in this study only comprised a reduced or absent pigment network without globules, as observed by Al Refu.[12] The cause of the plethora of pigmentary patterns in PV is debatable. Hypopigmentation is probably due to the cytotoxic effect of Malassezia on melanocytes, lipoperoxidation, or fungal scales, and pityriacitrin acting as sunscreens.[12,13,14] Various combinations of large melanosomes, increased tonofilaments in the stratum granulosum, and hyperkeratosis along with increased melanization due to underlying inflammation may cause hyperpigmentation.[13,14] Possibly, large melanosomes could cause dots, pigmentary network accentuation, and clods/blotches, whereas hyperkeratosis containing melanosomes, increased tonofilaments, and immunity stimulating inflammation may cause more diffuse pigmentation. However, this hypothesis needs to be tested histologically. Well-defined CH was less frequent than noted by Kaur.[3] Madarkar has noted this finding in only 4/50 patients.[9] Hyperpigmentary halos around hypopigmentation was much commoner than the converse similar like Kaur’s observations.[3]

Scaling is characteristic of PV and indicates active infection, unlike pigmentary changes.[2,3,4,9,15] In our study, scaling was universal, even without scratching, unlike previous studies. The fine, branny scale with follicular localization helps to eliminate differentials such as leprosy, and vitiligo. Resolution of scaling may indicate therapeutic response.[4] Predominant perifollicular scaling in this study contrass with previous studies where crease and patchy scaling predominated.[3,4,12] In fact, crease scaling was the least common in hypopigmented lesions. Non-crease interfollicular scales were commoner in hypopigmented PV (similar to Mathur’s observations) signifying that crease scaling may not be consistent.[4] Crease scales were commoner in hyperpigmented lesions similar to Mathur’s observations.[4] Double-edged crease scales have been described as being characteristic of pityriasis versicolor.[13] Differences in scaling patterns between clinically hypopigmented and hyperpigmented lesions could be due to fungal distribution in skin creases manifesting as scaling. Sweat and sebum in skin creases provide a pabulum for Malassezia, which may account for scaling. Slight preponderance of follicular scale in facial lesions could be due to a greater number of folliculosebaceous units and seborrhea. In all cases, scaling was better appreciated on polarized dermoscopy. Possibly, light reflected from the stratum corneum overwhelms the visual perception of fine scales in PV on non-polarized dermoscopy [Figures 2a and b].

Vascular features were common, unlike in previous studies. While Kaur and Madarkar have not described these, Mathur describes vascular features only in hypopigmented lesions since hyperpigmentation obscures underlying vascular patterns.[3,4,9] However, we noted more vascular features in hyperpigmented lesions, and no statistical difference was noted between hypopigmented and hyperpigmented lesions. Dermoscopic blush was the most common pattern, unlike Mathur, who noted linear vessels.[4] Interestingly, vascular features were observed even without scratching the lesions and without clinical erythema except in four lesions. Hyperemia may stimulate melanogenesis, contributing to hyperpigmented lesions.[14] Although vascularity would be expected to be associated with inflammation and consequent pruritus, no such correlation was noted in this study. Vascularity is evoked by inflammation due to Malassezia, which although restricted to the stratum corneum, is associated with dilated vessels and lymphocytic infiltrate in PV.[7,9,15,16,17] Besides, the role of Malassezia in causing koebnerization of psoriasis is known.[18] Possibly, cytokines released due to the pathogenic transformation of Malassezia, metabolic products of Malassezia, and consequent inflammatory infiltrate contribute to inflammation. Since vascularity and scaling increased in tandem, both lesionally and perilesionally, inflammation may partly contribute to scaling.

Larger proportions of lesions with both hyperpigmented and hypopigmented features had accentuated skin markings, due to a combination of pigmentary and scaling findings unlike Mathur, who noted predominant attenuation.[4] Obscured acrosyringial orifices, which were commoner than accentuation in hyperpigmented and hypopigmented lesions, have not been described previously and, in this study, were also due to pigmentary and scaly features.

Few series describe perilesional dermoscopic features.[3,12] Mathur described satellite lesions radiating from hair follicles.[4] In this study, these clinically normal areas did not fluoresce under Wood’s lamp. These features may constitute dermoscopic features of early PV due to the spread of lesions. Considering perilesional pigmentary changes, mechanisms similar to lesional pigmentation may be operative.[14] Perifollicular/follicular scale was preponderantly perilesionally suggesting that infection commences around/in hair follicles. Longer disease duration enabled Malassezia to spread to hair follicles perilesionally. Despite hyperpigmented lesions purportedly having a higher fungal load, perilesional features (except vascular changes) were commoner around hypopigmented lesions when compared with unaffected areas of normal skin on the same area (on KOH mount and Wood’s lamp examination).[4,15] Immunologic factors due to higher fungal load may contain the spread of infection in hyperpigmented lesions. Vascularity was higher around hyperpigmented lesions (although not statistically significant) supporting this premise. Since the intensity of perilesional pigmentary alteration, scaling, or vascularity did not increase with lesional intensity, the immune response could be active in trying to contain the infection. The presence of perilesional changes with KOH negativity as in our patients may indicate the need for closer observation to ascertain disease extension. Close contacts of patients may also be examined for such early features in order that early treatment be initiated.

Limitations of this study comprise lack of histopathologic correlation, relatively small sample sizes of immunosuppressed patients, lesions with clinically mixed pigmentation and erythematous lesions, thigh lesions, high attrition rate (precluding meaningful statistical analysis of dermoscopic features on follow-up), and absence of lower Fitzpatrick’s skin types. The absence of a non-PV control group to compare and assess the study’s findings including the specificity of crease and follicular scaling in PV is another limitation. Ultraviolet light dermoscopy would improve diagnostic accuracy. Future studies could also focus on the role of inflammation and T lymphocyte immunophenotypes in disease resolution/propagation. Assessing fungal species and load by colony forming units on culture in hyperpigmented and hypopigmented lesions, lesions with dermoscopic vascular patterns, types of scales and correlating with scaling and vascular patterns, and intensity with a therapeutic response may be of interest.

Conclusion

Dermoscopic patterns offer valuable clues to diagnose and appropriately treat PV, especially in case of diagnostic confusion in this usually indolent infection. Perilesional dermoscopic features may constitute evidence of subclinical spread. Dermoscopy may also reassure patients about disease inactivity since, after the resolution of scaling, pigmentary changes tend to persist longer but gradually resolve. Persistent scaling indicates the need for continued therapy. The role of immunity and the genetic background needs further investigation since the sizeable number of lesions with vascular findings may suggest failure of immune clearance. Such research may predict therapeutic response and lead to newer, more effective treatment modalities.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.